MTA2 promotes HCC progression through repressing FRMD6, a key upstream component of hippo signaling pathway
Autor: | Chengjian Guan, Xinjin Gu, Zhenyu Chang, Rong Liu |
---|---|
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male Carcinoma Hepatocellular Biophysics Kaplan-Meier Estimate Mice SCID Biology Protein Serine-Threonine Kinases Malignancy Biochemistry Histone Deacetylases Metastasis 03 medical and health sciences 0302 clinical medicine Carcinoma medicine Animals Humans Hippo Signaling Pathway MTA2 Molecular Biology Gene Regulation of gene expression Hippo signaling pathway Liver Neoplasms Membrane Proteins Cell Biology Hep G2 Cells medicine.disease Xenograft Model Antitumor Assays Gene Expression Regulation Neoplastic Repressor Proteins Cytoskeletal Proteins 030104 developmental biology RNAi Therapeutics 030220 oncology & carcinogenesis Hepatocellular carcinoma Cancer research Disease Progression Signal Transduction |
Zdroj: | Biochemical and biophysical research communications. 515(1) |
ISSN: | 1090-2104 |
Popis: | Discerning oncogenic drivers from passengers remains a major effort in understanding of the essence of the initiation and development of hepatocellular carcinoma (HCC), the most common primary liver malignancy and the third leading cause of cancer mortality worldwide. Here we report that MTA2, Metastasis Associated 1 Family Member 2, is significantly up-regulated in HCC. We show that high level of MTA2 expression is strongly correlated with advanced pathological stages and poor overall survival of the patients. Genome-wide identification of the transcriptional targets of MTA2 by ChIP-seq indicates that MTA2 represses a cohort of genes including FRMD6 that are critically involved in the growth and mobility of HCC. We demonstrate that the MTA2 promotes the proliferation and metastasis of HCC in vitro and in vivo through suppressing Hippo signaling pathway. Together, these results reveal a key role for the MTA2-FRDM6-Hippo axis in human hepatocarcinogenesis. |
Databáze: | OpenAIRE |
Externí odkaz: |